Laboratory, Endocrine, & Neurotransmitter Symposium

August 28-30, 2020

Bellevue, WA

Gain additional clinical insight and treatment considerations to evaluate some of the most prevalent and challenging conditions that patients present with, including depression, anxiety, altered mental focus and stamina, sexual dysfunction, sleep disturbances, addictions and dependencies, weight management, and chronic disease. Get notified when registration goes live!


Wellness Wednesday

Webinar Series

Belly Fat and Elevated Androgens in Women

By: Heather Hydzik, ND

April 1st, 2020

In this month's webinar, you will review insulin resistance, metabolic syndrome and PCOS in women, obtain in-depth understanding of hormonal and metabolic pathways associated with elevated androgens in women, and learn about adipose tissue and its role in hormonal imbalance. Attendees will also obtain current testing and assessment strategies and learn successful treatment considerations to employ in practice immediately. Sign up today!



Interpreting and Applying GI360 Test Data: Identifying the 3 Stages of GI Dysfunction

By: Dan Kalish DC and Julia Malkowski ND, DC

April 16th, 2020 at 3 PM PST

Why is GI testing so important for every patient, not just those patients that present with GI symptoms? And why is it imperative to consider profiles that include a variety of complementary testing methodologies, including PCR and culture? Learn about the practical application of the Doctor’s Data GI360 profile, with a hands-on approach.


GUS Activity, Diet and Low IQ


By David Quig, PhD | March 31, 2020

Early research revealed the potential adverse consequences associated with high total fecal β-glucuronidase (GUS) activity. After a long hiatus, advanced research indicates that there are hundreds of colonic microbial GUSs that have distinct structural and functional characteristics. The clinical interpretations and interventions remain mostly the same for reported fecal levels of total GUS activity, but much “behind the curtain” is yet to be fully understood.

Gastrointestinal GUSs release activated xenobiotic and endobiotic β-glucuronides produced via integral hepatic Phase II detoxification. The GUS activity facilitates enteroheptic resorption of the aglycone moieties that the body has attempted to excrete. As such, GUSs may significantly affect pharmacokinetics and toxicokinetics of many chemical entities, increasing their exposure life times in the host. A classic example is GUS-induced delayed elimination of endocrine-disrupting bisphenol A. Higher fecal GUS activity has been associated with higher circulating estrogens and lower fecal excretion of estrogens (premenopausal). Less appreciated is the beneficial role of GUSs to “recycle” and bioactivate important dietary components such as flavonoids. De-glucuronidation of certain flavonoids facilitates their systemic anti-inflammatory, antioxidant, antiviral and antitumor effects, implicating the importance of maintaining a healthy level of GUS activity.

Bacteria from all the major phyla in the human GI microbiome express GUS activity. A recent landmark study demonstrated that GI microbiota collectively express hundreds of distinct GUSs that have diverse structures and catalytic efficiencies, with potential favorable and unfavorable effects. Opportunistic and pathogenic bacteria (i.e. Proteobacteria such as Escherichia coli and Klebsiella Pneumoniae) appear to be associated with GUS-induced xenobiotic injury to the epithelium . It should be noted that all of the studied microbial GUSs appear to have sufficient catalytic capacity to release various xenobiotics from their respective glucuronides, and GUS is also produced by GI epithelial cells and hepatocytes. Much more extensive research is required before testing might possibly be available to more specifically assess GUS activities in fecal samples.

GUS activity can be modulated by diet, and bacterial abundance and diversity. High-fat, high protein, and low soluble fiber diets are associated with higher GUS activity. Compared to a strict vegetarian diet, a diet containing grilled/smoked meat may be associated with induction of GUS activity, and extended circulating half-life of a meat-derived carcinogen (IQ)*. Other carcinogenic chemicals induce GUS expression.

Clinical considerations to lower high GUS activities include modification of diet; a low fat, low meat and high fiber diet, such as consumed by strict vegetarians, may be associated with lower GUS activity compared to a typical “Western diet.” Inulin has been shown to decrease GUS activity, and IQ*-induced DNA damage in colon and liver cells (rats). Specific probiotics containing Lactobacillus species; sustained use of a specific strain of Lactobacillus rhamnosus GG lowered GUS activity in healthy subjects in the absence of dietary modification. Keep the bowels moving. Consider Ca-D-glucarate; at least 1,500 mg/day in divided doses with food. About 30% of ingested D-glucarate is converted to the short-lived, low affinity inhibitor (D-glucaro-1,4-lactone). Mitigate exposure to chemical source(s) of induction of GUS, and consider assessment of the levels of sex steroidal hormones and their metabolites.


1.Dashnyam P et al. β-Glucuronidases of opportunistic bacteria are the major contributors to xenobiotic-induced toxicity in the gut. Sci Rep(2018)8:16372 doi: 10.1038/s41598-018-34678-z

2.Kwa M et al. The intestinal microbiome and estrogen-positive female breast cancer. J Nat Cancer Inst(2015)108 doi: 10.1093/jnci/djw029

3.Sunkata R et al. Chemopreventivepotential of probiotic. Food Nutr Sci(2014)55:1800-9 doi: 10.4236/fns.2014.518194

*IQ is 2-amino-3-methylimidazo[4,5-f]quinolone

Disclaimer: All information given about health conditions, treatment, products, and dosages are for educational purposes only and do not constitute medical advice.


The GI360™ Profile: an innovative, comprehensive and clinically-applicable stool profile, utilizing multiplex PCR molecular technology coupled with growth-based culture and ID by MALDI-TOF, sensitive biochemical assays and microscopy to detect and assess the status of pathogens, viruses, parasites and bacteria that may be contributing to acute or chronic gastrointestinal symptoms and disease.